Atherosclerosis, colloquially called arterial calcification, is one of the most serious and most frequent diseases in the Western world. Until now, it has not been possible to fully clarify its aetiopathogenesis. For example, numerous exogenous and endogenous noxac and diseases are held responsible for triggering or promoting atherosclerosis. Examples hereof are hypertonia, hyperlipidaemia, hyperfibrinogenaemia, diabetes mellitus, toxins, nicotine, antigen-antibody complexes, inflammation, etc. An increased lipid level in the blood; especially hypercholesterolaemia, i.e. raised cholesterol levels in the blood (>200 mg/dl), is without doubt a significant risk factor. One meaningful approach to the prophylaxis and, to a certain extent, therapy of this disease and its consequences (cardiac infarction, cerebral and peripheral circulatory disturbance, etc.) has so far been to bring down raised plasma lipid levels, especially raised plasma cholesterol levels.
Like other arteries, the coronary artery and especially the major coronary arterial branches may be affected by atherosclerosis. Coronary sclerosis which results in stenosis of the coronary flow canal or which, through the additional formation of thrombi, may cause partial or complete occlusion of the branches of the coronary artery is the most important cause of coronary heart disease. Proven risk factors are: smoking, excess weight, hypertonia, hyperlipoproteinaemia and diabetes mellitus. These factors must be taken into account for prophylaxis.
Plasma lipids are neutral fats, phospholipidos, cholesterol, cholesterol esters and free fatty acids. Since lipids arc insoluble in water, they are transported in the blood not in free form, but rather in the form of so-called lipoproteins, i.e. bound to carrier proteins. The lipoproteins are subdivided into chylomicrons very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), intermediate-density lipoproteins (IDL) and high-density with pyruvate should eliminate this irritating and toxic potential of these activated blood cells.
In another embodiment, the metal salt of the lactate is used as an alkali metal salt or alkaline earth metal salt of the lactate, preferably as calcium lactate. Calcium is capable thereby of binding the bile acids which have entered the intestine via the enterohepatic cycle. This reduces re-transport to the liver. In order to maintain the balance in the enterohepatic cycle, a greater amount of cholesterol must be converted in the liver to bile acid. This results in a decrease of the plasma cholesterol level. Not only does this have an impact on the generation of sclerotic arteries, but it also at the same time removes a possible main cause of artherosclerosis from the body, which further decreases the risk of atherosclerosis.
Calcium constitutes an important nutrient for normal growth and development. It helps in regulating the cell function and is an indispensable structural component of the bone. Since the body is not capable of producing calcium itself, it must be taken up through food. About 25 to 35% of the calcium taken up through food is absorbed in the intestine, mostly in the duodenum and in the jejunum, the remaining 65 to 75% of the calcium supplied are not used and thus excreted. Therefore, approximately two thirds to three fourths of the calcium supply are available for binding the bile acids and thus for the reducing the cholesterol level. On the other hand, the absorbed amount helps to improve the skeleton and thus to prevent osteoporosis.
Calcium lactate is characterised by good solubility. This permits improved calcium absorption, which increases the positive effect on the skeleton. Thereby, the absolute amount of calcium available in the intestine is reduced, this can, however, be easily counteracted by increasing the amount uptaken. Moreover, the amount of calcium in the human body is continuously subject to equilibration by means of absorption and secretion. The increased amount of calcium taken up is thus excreted for the most part and can possibly further increase, from the inside, the binding and, thus, secretion of bile acids.
In another embodiment according to the invention, a micro-encapsulation of the lactate metal salt or of a pharmaceutical composition made therefrom has proven to be especially advantageous. The micro-encapsulation can, for example, be carried out as described in the laid-open patent specifications DE 193 54 749 A1 and DE 100 08 880 A1 as well as in the German utility model DE 296 23 285 U1. In this process, the lactate salt is, for example, firmly enclosed in a capsule of a polysaccharide such as, e.g., alginate. In order to ensure that the capsule, which may be indigestible, does not prevent release of the lactate, which would make physiological utilisation by the organism impossible, a lipoproteins (HDL). Whilst the main component of LDLs is cholesterol, the HDLs have an especially high protein content and a comparatively low cholesterol content HDLs are able to take up cholesterol deposited on vessel walls and to pass it on to the IDLs.
Chylomicrons are produced during fat resorption in the intestinal wall they then come into the blood via the lymph and, after cleavage of the triglycerides by the lipoprotein lipase, release the so-called clearing factor, fatty acids, to fat tissues (for storage) and to the muscles (as a fuel). The remnants, which have a high cholesterol ester content, are now bound to a special receptor (remnant receptor) that is found only in liver cells, and are transported into the liver cell by this receptor. The cholesterol received by the liver cell is, on the one hand, converted to bile acids, which are then released into the intestine with the bile, and, on the other hand, is transported back into the circulation together with apoproteins, phospholipids and triglycerides in the form of VLDL.
The object of the present invention is to provide a pharmaceutical composition suitable for the treatment and/or prophylaxis of atherosclerosis and/or the prophylaxis or treatment of diseases caused by atherosclerosis.